The role of cagApositivestrains in patients with oesophageal adenocarcinoma

Different studies hint on a protective role of Helicobacter pylori infection - especially cagA+-strains - against the development of oesophageal adenocarcinoma.

The incidence of oesophageal adenocarcinoma increased over the last years [59] reaching 4-12 per 100.000. This is in contrast to the decreasing incidence of non-cardia gastric cancer (Fig. 3), [63].

Quddus et al did not find any Helicobacter pylori infected in 19 patients with Barrett's adenocarcinoma [60]. In a larger study population Helicobacter pylori again has been identified in significantly higher proportion of patients with benign Barrett's oesophagus than in those with dysplastic Barrett's oesophagus or Barrett's adenocarcinoma (34% vs. 17%) [61].

A multicenter study did not find a difference in the prevalence of Helicobacter pylori infection in patients with oesophageal adenocarcinoma when compared to age- and sex-matched controls. However infection with the cagA+ strain of the bacteria resulted in a reduced odds ratio for developing oesophageal adenocarcinoma [57]. These results have been confirmed in a smaller study by Vicari et al [5] and may be explained by Helicobacter pylori induced apoptosis in Barrett derived oesophageal adenocarcinoma cells which is mainly dependent on the presence of the cagA and picB/cagE gene products [62].

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